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  1. Article ; Online: Identification of an Epigenetic Signature of Osteoporosis in Blood DNA of Postmenopausal Women.

    Cheishvili, David / Parashar, Surabhi / Mahmood, Niaz / Arakelian, Ani / Kremer, Richard / Goltzman, David / Szyf, Moshe / Rabbani, Shafaat A

    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    2021  Volume 36, Issue 11, Page(s) 2285–2286

    Language English
    Publishing date 2021-07-05
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 632783-7
    ISSN 1523-4681 ; 0884-0431
    ISSN (online) 1523-4681
    ISSN 0884-0431
    DOI 10.1002/jbmr.4392
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2142: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  2. Article ; Online: Identification of an Epigenetic Signature of Osteoporosis in Blood DNA of Postmenopausal Women.

    Cheishvili, David / Parashar, Surabhi / Mahmood, Niaz / Arakelian, Ani / Kremer, Richard / Goltzman, David / Szyf, Moshe / Rabbani, Shafaat A

    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    2018  Volume 33, Issue 11, Page(s) 1980–1989

    Abstract: Osteoporosis is one of the most common age-related progressive bone diseases in elderly people. Approximately one in three women and one in five men are predisposed to developing osteoporosis. In postmenopausal women, a reduction in BMD leads to an ... ...

    Abstract Osteoporosis is one of the most common age-related progressive bone diseases in elderly people. Approximately one in three women and one in five men are predisposed to developing osteoporosis. In postmenopausal women, a reduction in BMD leads to an increased risk of fractures. In the current study, we delineated the DNA methylation signatures in whole blood samples of postmenopausal osteoporotic women. We obtained whole blood DNA from 22 normal women and 22 postmenopausal osteoporotic women (51 to 89 years old) from the Canadian Multicenter Osteoporosis Study (CaMos) cohort. These DNA samples were subjected to Illumina Infinium human methylation 450 K analysis. Illumina 450K raw data were analyzed by Genome Studio software. Analysis of the female participants with early and advanced osteoporosis resulted in the generation of a list of 1233 differentially methylated CpG sites when compared with age-matched normal women. T test, ANOVA, and post hoc statistical analyses were performed, and 77 significantly differentially methylated CpG sites were identified. From the 13 most significant genes, ZNF267, ABLIM2, RHOJ, CDKL5, and PDCD1 were selected for their potential role in bone biology. A weighted polygenic DNA methylation score of these genes predicted osteoporosis at an early stage with high sensitivity and specificity and correlated with measures of bone density. Pyrosequencing analysis of these genes was performed to validate the results obtained from Illumina 450 K methylation analysis. The current study provides proof of principal for the role of DNA methylation in osteoporosis. Using whole blood DNA methylation analysis, women at risk of developing osteoporosis can be identified before a diagnosis of osteoporosis is made using BMD as a screening method. Early diagnosis will help to select patients who might benefit from early therapeutic intervention. © 2018 American Society for Bone and Mineral Research.
    MeSH term(s) Aged ; Aged, 80 and over ; Biomarkers/blood ; Cluster Analysis ; CpG Islands/genetics ; DNA/blood ; DNA Methylation/genetics ; Epigenesis, Genetic ; Female ; Genome, Human ; Humans ; Middle Aged ; Osteoporosis/blood ; Osteoporosis/genetics ; Postmenopause/blood ; Postmenopause/genetics ; ROC Curve ; Reproducibility of Results
    Chemical Substances Biomarkers ; DNA (9007-49-2)
    Language English
    Publishing date 2018-07-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632783-7
    ISSN 1523-4681 ; 0884-0431
    ISSN (online) 1523-4681
    ISSN 0884-0431
    DOI 10.1002/jbmr.3527
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2142: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: DNA methylation signatures of breast cancer in peripheral T-cells.

    Parashar, Surabhi / Cheishvili, David / Mahmood, Niaz / Arakelian, Ani / Tanvir, Imrana / Khan, Haseeb Ahmed / Kremer, Richard / Mihalcioiu, Catalin / Szyf, Moshe / Rabbani, Shafaat A

    BMC cancer

    2018  Volume 18, Issue 1, Page(s) 574

    Abstract: Background: Immune surveillance acts as a defense mechanism in cancer, and its disruption is involved in cancer progression. DNA methylation reflects the phenotypic identity of cells and recent data suggested that DNA methylation profiles of T cells and ...

    Abstract Background: Immune surveillance acts as a defense mechanism in cancer, and its disruption is involved in cancer progression. DNA methylation reflects the phenotypic identity of cells and recent data suggested that DNA methylation profiles of T cells and peripheral blood mononuclear cells (PBMC) are altered in cancer progression.
    Methods: We enrolled 19 females with stage 1 and 2, nine with stage 3 and 4 and 9 age matched healthy women. T cells were isolated from peripheral blood and extracted DNA was subjected to Illumina 450 K DNA methylation array analysis. Raw data was analyzed by BMIQ, ChAMP and ComBat followed by validation of identified genes by pyrosequencing.
    Results: Analysis of data revealed ~ 10,000 sites that correlated with breast cancer progression and established a list of 89 CG sites that were highly correlated (p < 0.01, r > 0.7, r < - 0.7) with breast cancer progression. The vast majority of these sites were hypomethylated and enriched in genes with functions in the immune system.
    Conclusions: The study points to the possibility of using DNA methylation signatures as a noninvasive method for early detection of breast cancer and its progression which need to be tested in clinical studies.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor/genetics ; Breast Neoplasms/diagnosis ; Breast Neoplasms/genetics ; Breast Neoplasms/immunology ; Breast Neoplasms/pathology ; Case-Control Studies ; DNA Methylation/immunology ; Disease Progression ; Epigenesis, Genetic ; Female ; Healthy Volunteers ; Humans ; Immunologic Surveillance/genetics ; Middle Aged ; Oligonucleotide Array Sequence Analysis ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
    Chemical Substances Biomarkers, Tumor
    Language English
    Publishing date 2018-05-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 2041352-X
    ISSN 1471-2407 ; 1471-2407
    ISSN (online) 1471-2407
    ISSN 1471-2407
    DOI 10.1186/s12885-018-4482-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: S-adenosylmethionine blocks osteosarcoma cells proliferation and invasion in vitro and tumor metastasis in vivo: therapeutic and diagnostic clinical applications.

    Parashar, Surabhi / Cheishvili, David / Arakelian, Ani / Hussain, Zahid / Tanvir, Imrana / Khan, Haseeb Ahmed / Szyf, Moshe / Rabbani, Shafaat A

    Cancer medicine

    2015  Volume 4, Issue 5, Page(s) 732–744

    Abstract: Osteosarcoma (OS) is an aggressive and highly metastatic form of primary bone cancer affecting young children and adults. Previous studies have shown that hypomethylation of critical genes is driving metastasis. Here, we examine whether hypermethylation ... ...

    Abstract Osteosarcoma (OS) is an aggressive and highly metastatic form of primary bone cancer affecting young children and adults. Previous studies have shown that hypomethylation of critical genes is driving metastasis. Here, we examine whether hypermethylation treatment can block OS growth and pulmonary metastasis. Human OS cells LM-7 and MG-63 were treated with the ubiquitous methyl donor S-adenosylmethionine (SAM) or its inactive analog S-adenosylhomocystine (SAH) as control. Treatment with SAM resulted in a dose-dependent inhibition of tumor cell proliferation, invasion, cell migration, and cell cycle characteristics. Inoculation of cells treated with 150 μmol/L SAM for 6 days into tibia or via intravenous route into Fox Chase severe combined immune deficient (SCID) mice resulted in the development of significantly smaller skeletal lesions and a marked reduction in pulmonary metastasis as compared to control groups. Epigenome wide association studies (EWAS) showed differential methylation of several genes involved in OS progression and prominent signaling pathways implicated in bone formation, wound healing, and tumor progression in SAM-treated LM-7 cells. Real-time polymerase chain reaction (qPCR) analysis confirmed that SAM treatment blocked the expression of several prometastatic genes and additional genes identified by EWAS analysis. Immunohistochemical analysis of normal human bone and tissue array from OS patients showed significantly high levels of expression of one of the identified gene platelet-derived growth factor alpha (PDGFA). These studies provide a possible mechanism for the role of DNA demethylation in the development and metastasis of OS to provide a rationale for the use of hypermethylation therapy for OS patients and identify new targets for monitoring OS development and progression.
    MeSH term(s) Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacology ; Biopsy ; Bone Neoplasms/diagnosis ; Bone Neoplasms/drug therapy ; Bone Neoplasms/genetics ; Bone Neoplasms/pathology ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; DNA Methylation/drug effects ; Epigenomics ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Male ; Mice ; Neoplasm Metastasis ; Osteosarcoma/diagnosis ; Osteosarcoma/drug therapy ; Osteosarcoma/genetics ; Osteosarcoma/pathology ; S-Adenosylmethionine/administration & dosage ; S-Adenosylmethionine/pharmacology ; Tumor Stem Cell Assay
    Chemical Substances Antineoplastic Agents ; S-Adenosylmethionine (7LP2MPO46S)
    Language English
    Publishing date 2015-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2045-7634
    ISSN (online) 2045-7634
    DOI 10.1002/cam4.386
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Pharmacological methyl group donors block skeletal metastasis in vitro and in vivo.

    Shukeir, Nicholas / Stefanska, Barbara / Parashar, Surabhi / Chik, Flora / Arakelian, Ani / Szyf, Moshe / Rabbani, Shafaat A

    British journal of pharmacology

    2015  Volume 172, Issue 11, Page(s) 2769–2781

    Abstract: Background and purpose: DNA hypomethylation was previously implicated in metastasis. In the present study, we examined whether methyl supplementation with the universal methyl donor S-adenosylmethionine (SAM) inhibits prostate cancer associated skeletal ...

    Abstract Background and purpose: DNA hypomethylation was previously implicated in metastasis. In the present study, we examined whether methyl supplementation with the universal methyl donor S-adenosylmethionine (SAM) inhibits prostate cancer associated skeletal metastasis.
    Experimental approach: Highly invasive human prostate cancer cells PC-3 and DU-145 were treated with vehicle alone, S-adenosylhomocysteine (SAH) or SAM and their effects on tumour cell proliferation, invasion, migration and colony formation were monitored. For in vivo studies, control (SAH) and SAM-treated PC-3 cells were injected into the tibia of Fox chase SCID mice and skeletal lesions were determined by X-ray and μCT. To understand possible mechanisms involved, we delineated the effect of SAM on the genome-wide methylation profile of PC-3 cells.
    Key results: Treatment with SAM resulted in a dose-dependent inhibition of tumour cell proliferation, invasion, cell migration, colony formation and cell cycle characteristics. Animals injected with 250 μM SAM-treated cells developed significantly smaller skeletal lesions, which were associated with increases in bone volume to tumour volume ratio and connectivity density as well as decreased trabecular spacing. Genome-wide methylation analysis showed differential methylation in several key signalling pathways implicated in prostate cancer including the signal transducer and activator of transcription 3 (STAT3) pathway. A selective STAT3 inhibitor decreased tumour cell invasion, effects which were less pronounced as compared with SAM.
    Conclusions and implications: These studies provide a possible mechanism for the role of DNA demethylation in the development of skeletal metastasis and a rationale for the use of hypermethylation pharmacological agents to impede the development and progression of skeletal metastasis.
    MeSH term(s) Adenocarcinoma/genetics ; Adenocarcinoma/secondary ; Animals ; Bone Neoplasms/genetics ; Bone Neoplasms/secondary ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Movement/genetics ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; DNA Methylation/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; In Vitro Techniques ; Male ; Mice ; Mice, SCID ; Neoplasm Invasiveness/genetics ; Neoplasm Metastasis/genetics ; Neoplasm Transplantation ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; S-Adenosylmethionine/pharmacology ; Tibia/diagnostic imaging ; Tibia/drug effects ; X-Ray Microtomography
    Chemical Substances S-Adenosylmethionine (7LP2MPO46S)
    Language English
    Publishing date 2015-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.13102
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uf I Zs.146: Show issues Location:
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